Motor training strengthens corticospinal suppression during movement preparation

Movement preparation involves a broad suppression in the excitability of the corticospinal pathway, a phenomenon called preparatory suppression. Here, we show that motor training strengthens preparatory suppression and that this strengthening is associated with faster reaction times. Our findings highlight a key role of preparatory suppression in training-driven behavioral improvements.

Only the fastest corticospinal fibers contribute to beta corticomuscular coherence

ABSTRACTA common way to study human corticospinal transmission is with transcranial magnetic stimulation. However, this is biased to activity in the fastest conducting axons. It is unclear whether conclusions obtained in this context are representative of volitional activity in mild-to-moderate contractions. A possible alternative to overcome this limitation is to study the corticospinal transmission of endogenously generated brain activity. Here we study the transmission speeds of cortical beta rhythms travelling to the muscles during steady contractions. To do this, we introduce new methods to improve delay estimates in the corticomuscular transmission of beta rhythms, and which we validate both in simulations and experimentally. Applying these approaches to experimental data from humans, we show that corticomuscular beta transmission delays are only 1-2ms longer than expected from the fastest corticospinal pathway. Simulations using realistic distributions of the conduction velocities for descending axons projecting to lower motoneurons suggest two scenarios that can explain these results: either a very small fraction of only the fastest corticospinal axons selectively transmit beta activity, or else the entire pool does. The implications that these two scenarios have for our understanding of corticomuscular interactions are discussed in the final part of this manuscript.SIGNIFICANCEWe present and validate an improved methodology to measure the delay in the transmission of cortical beta activity to tonically active muscles. The estimated corticomuscular beta transmission delays which this yields are remarkably similar to those expected from transmission in the fastest corticospinal axons. A simulation of beta transmission along a pool of corticospinal axons using a realistic distribution of fiber diameters suggests two possible mechanisms by which fast corticomuscular transmission is achieved: either a very small fraction of descending axons transmits beta activity to the muscles or, alternatively, the entire population does and natural cancellation of slow channels occurs due to the distribution of axon diameters in the corticospinal tract.

Navigated transcranial magnetic stimulation of the primary somatosensory cortex evokes motor potentials in healthy humans’ flexor carpi radialis muscle - A pilot study

Background: Although previous studies targeted S1 by TMS to investigate its effect on the corticospinal pathway, there is no evidence if such stimuli produced by TMS would distinctly be restricted to it and not reach M1 interneurons adjacent to S1.Aim: We hypothesized that S1 vs. M1 stimulation-induced MEPs would be similar but smaller and less variable due to the focality of the magnetic pulse, considering that even if TMS is neuronavigated, the magnetic field is not selective enough and reaches M1 interneurons.Method: Healthy volunteers (n = 8, 2 females, age: 29.9 ± 5.49y) received single-pulse TMS over each hemisphere at each intensity of 90, 100, 110, and 120% of rMT in a randomized order. MEPs from the contralateral FCR were recorded.Results: We found no interhemispheric differences, but larger peak-to-peak amplitudes and variability of MEPs after M1 as compared to S1 stimulation. However, latency and waveforms of MEPs did not differ between S1 vs. M1 stimulation supporting the idea that TMS over S1 is not selective enough and can excite M1 interneurons thus producing MEPs on the contralateral FCR.Interpretation: Future studies should carefully consider these results when targeting S1 with TMS even if using a neuronavigation system.

High-intensity, low-frequency repetitive transcranial magnetic stimulation enhances excitability of the human corticospinal pathway

In this study, we present a novel, intensity-dependent repetitive transcranial magnetic stimulation (rTMS) protocol that induces lasting, plastic changes within the corticospinal tract. High-intensity rTMS at a frequency of 0.1 Hz induces facilitation of motor evoked potentials (MEPs) lasting at least 35 min. Additionally, these changes are not limited only to small MEPs but occur throughout the recruitment curve. Finally, facilitation of MEPs following high-intensity rTMS does not appear to be due to changes in intracortical inhibition or facilitation.

Neurophysiological responses and adaptation following repeated bouts of maximal lengthening contractions in young and older adults

A bout of maximal lengthening contractions is known to produce muscle damage, but confers protection against subsequent damaging bouts, with both tending to be lower in older adults. Neural factors contribute to this adaptation, but the role of the corticospinal pathway remains unclear. Twelve young (27 ± 5 yr) and 11 older adults (66 ± 4 yr) performed two bouts of 60 maximal lengthening dorsiflexions 2 weeks apart. Neuromuscular responses were measured preexercise, immediately postexercise, and at 24 and 72 h following both bouts. The initial bout resulted in prolonged reductions in maximal voluntary torque (MVC; immediately postexercise onward, P < 0.001) and increased creatine kinase (from 24 h onward, P = 0.001), with both responses being attenuated following the second bout ( P < 0.015), demonstrating adaptation. Smaller reductions in MVC following both bouts occurred in older adults ( P = 0.005). Intracortical facilitation showed no changes ( P ≥ 0.245). Motor-evoked potentials increased 24 and 72 h postexercise in young ( P ≤ 0.038). Torque variability ( P ≤ 0.041) and H-reflex size ( P = 0.024) increased, while short-interval intracortical inhibition (SICI; P = 0.019) and the silent period duration (SP) decreased ( P = 0.001) in both groups immediately postexercise. The SP decrease was smaller following the second bout ( P = 0.021), and there was an association between the change in SICI and reduction in MVC 24 h postexercise in young adults ( R = −0.47, P = 0.036). Changes in neurophysiological responses were mostly limited to immediately postexercise, suggesting a modest role in adaptation. In young adults, neural inhibitory changes are linked to the extent of MVC reduction, possibly mediated by the muscle damage–related afferent feedback. Older adults incurred less muscle damage, which has implications for exercise prescription. NEW & NOTEWORTHY This is the first study to have collectively assessed the role of corticospinal, spinal, and intracortical activity in muscle damage attenuation following repeated bouts of exercise in young and older adults. Lower levels of muscle damage in older adults are not related to their neurophysiological responses. Neural inhibition transiently changed, which might be related to the extent of muscle damage; however, the role of processes along the corticospinal pathway in the adaptive response is limited.

Changes in motor-evoked potential latency during grasping after tetraplegia

The corticospinal pathway contributes to the control of grasping in intact humans. After spinal cord injury (SCI), there is an extensive reorganization in the corticospinal pathway; however, its contribution to the control of grasping after the injury remains poorly understood. We addressed this question by using transcranial magnetic stimulation (TMS) over the hand representation of the motor cortex to elicit motor-evoked potentials (MEPs) in an intrinsic finger muscle during precision grip and power grip with the TMS coil oriented to induce currents in the brain in the latero-medial (LM) direction to activate corticospinal axons directly and in the posterior-anterior (PA) and anterior-posterior (AP) directions to activate the axon indirectly through synaptic inputs in humans with and without cervical incomplete SCI. We found prolonged MEP latencies in all coil orientations in both tasks in SCI compared with control subjects. The latencies of MEPs elicited by AP relative to LM stimuli were consistently longer during power compared with precision grip in controls and SCI subjects. In contrast, PA relative to LM MEP latencies were similar between tasks across groups. Central conduction time of AP MEPs was prolonged during power compared with precision grip in controls and SCI participants. Our results support evidence indicating that inputs activated by AP and PA currents are engaged to a different extent during fine and gross grasping in humans with and without SCI. NEW & NOTEWORTHY The mechanisms contributing to the control of hand function in humans with spinal cord injury (SCI) remain poorly understood. Here, we demonstrate for the first time that the latency of corticospinal responses elicited by transcranial magnetic stimulation anterior-posterior induced currents, relative to latero-medial currents, was prolonged during power compared with precision grip in humans with and without SCI. Gross grasping might represent a stragegy to engage networks activated by anterior-posterior currents after SCI.